Pathogen-induced tissue-resident memory T H 17 (T RM 17) cells amplify autoimmune kidney disease
| Autor: | Leon U. B. Enk, Natascha E. Stumpf, Yu Zhao, Milagros N. Wong, Ulf Panzer, Clemens D. Cohen, Daniel Reimers, Stefanie Klinge, Constantin Schmidt, Christian Krebs, Christian Kurts, M. Rosemblatt, Sarah Nuñez, Nicola Gagliani, Catherine Meyer-Schwesinger, Thorsten Wiech, Tabea Bertram, Jan-Hendrik Riedel, Patricia Bartsch, Joanna Schmid, Christoph Kilian, Sören Franzenburg, Tobias B. Huber, Stefan Bonn, Alina Borchers, Maja T. Lindenmeyer, Jan-Eric Turner, Martina Becker, Hans-Joachim Paust, Friedrich Koch-Nolte, Michael Rink, María Rosa Bono, Holger Rohde, Elion Hoxha, Michael Zinke, Victor G. Puelles, Hans-Willi Mittrücker, Malte Hellmig, Samuel Huber |
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| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine immunology [T-Lymphocyte Subsets] Immunology Mice Transgenic microbiology [Glomerulonephritis] Proinflammatory cytokine 03 medical and health sciences 0302 clinical medicine immunology [Autoimmune Diseases] immunology [Bacterial Infections] Candida albicans medicine Animals Humans Cytotoxic T cell ddc:610 immunology [Kidney] immunology [CD4-Positive T-Lymphocytes] Autoimmune disease Kidney biology business.industry Glomerulonephritis General Medicine immunology [Glomerulonephritis] medicine.disease biology.organism_classification immunology [Candidiasis] 030104 developmental biology medicine.anatomical_structure Renal pathology immunology [Antibodies Antineutrophil Cytoplasmic] Mice Inbred DBA business Immunologic Memory 030217 neurology & neurosurgery microbiology [Autoimmune Diseases] Kidney disease |
| Zdroj: | Science immunology 5(50), eaba4163-(2020). doi:10.1126/sciimmunol.aba4163 |
| ISSN: | 2470-9468 |
| DOI: | 10.1126/sciimmunol.aba4163 |
| Popis: | Although it is well established that microbial infections predispose to autoimmune diseases, the underlying mechanisms remain poorly understood. After infection, tissue-resident memory T (TRM) cells persist in peripheral organs and provide immune protection against reinfection. However, whether TRM cells participate in responses unrelated to the primary infection, such as autoimmune inflammation, is unknown. By using high-dimensional single-cell analysis, we identified CD4+ TRM cells with a TH17 signature (termed TRM17 cells) in kidneys of patients with ANCA-associated glomerulonephritis. Experimental models demonstrated that renal TRM17 cells were induced by pathogens infecting the kidney, such as Staphylococcus aureus, Candida albicans, and uropathogenic Escherichia coli, and persisted after the clearance of infections. Upon induction of experimental glomerulonephritis, these kidney TRM17 cells rapidly responded to local proinflammatory cytokines by producing IL-17A and thereby exacerbate renal pathology. Thus, our data show that pathogen-induced TRM17 cells have a previously unrecognized function in aggravating autoimmune disease. |
| Databáze: | OpenAIRE |
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